Invasive blood pressure measurement is important for hemodynamic monitoring and for providing intensive care to patients with shock in the ICU. This prospective study, aimed to investigate the difference between radial and femoral MAP in refractory shock patients receiving high-dose vasopressor therapy. This study found that MAP monitoring at the radial artery significantly underestimated the central arterial pressure as represented by the femoral artery. Nearly 60% of our refractory shock patients had significant radial-femoral MAP gradients, and MAPradial less than 65 mmHg was an independent risk factor associated with an increased MAP gradient.
Similar to previous studies, this study found disagreement between MAP obtained from the radial and femoral arteries in critically ill patients. Kim et al. demonstrated that the bias between MAPfemoral and MAPradial was 4.9 mmHg (95% LOA, -6.9 to 17) in septic shock patients 14. Previous study in 24 critically ill patients, in mixed ICU found that bias between femoral and radial MAP was 4.3 mmHg (95% LOA, -3.4 to 11.9)15.
On the other hand, Mignini et al. proposed that measurement of MAP at radial or femoral arteries is clinically interchangeable in critically ill patients. They found that MAPfemoral was higher than MAPradial but was not statistically significant, with a mean bias of 3±4 mmHg (95% LOA,16)16. A more recent study by Antal et al. also found that MAPfemoral and MAPradial had a good correlation and agreement in sepsis patients, with a bias of 1.4±4.7 mmHg (95% LOA, 18.3). The difference between our results and those studies may be related to the different study populations and severity of vasopressors used. Patients with refractory shock in this study were diagnosed with septic shock and required a very high dose of vasopressor (equivalent dose of norepinephrine 0.85 ug/kg/min). However, in the study by Antal et al., only half of their study population was diagnosed with septic shock and they received a lower dose of norepinephrine (0.14 ± 0.17 ug/kg/min) compared to this study.
There were conflicting results regarding the vasopressor dose-effect on the radial-femoral MAP gradients. Previous studies have reported that clinically radial-femoral MAP gradients are commonly observed in patients receiving high doses of norepinephrine administration13,14. Kim et al. showed that septic shock patients receiving norepinephrine < 0.1 ug/kg/min had a bias between MAPfemoral and MAPradial of 3 mmHg (95% LOA, -7.2 to 13.1); however, the large discrepancies between MAP were found in patients receiving norepinephrine ≥ 0.1 ug/kg/min, with a bias of up to 6.2 mmHg (95% LOA -6.0 to 18.3). In contrast, other studies have found that norepinephrine dose was not associated with the MAP gradient. Mignini et al. demonstrated that the bias of MAPradial and MAPfemoral was not different between patients receiving high and low dose of vasoactive agents (high vasoactive dose defined as norepinephrine or epinephrine ≥ 0.1 ug/kg/min or dopamine ≥ 10 ug/kg/min). This is consistent with a study in sepsis patients showing that the norepinephrine dose did not the influence the radial-femoral MAP difference17. The results of this study support the statement that norepinephrine dose does not influence the radial-femoral MAP gradient.
This study found a high prevalence of clinically significant MAP gradients between the radial and femoral arteries in patients with refractory shock. This is similar to previous studies reporting that 62% of critically ill patients had a MAP difference of at least 5 mmHg and 27%-29% of patients had a MAP gradient ≥ 10 mmHg14,15. Although, the factors associated with radial-femoral MAP gradients have been extensively investigated, the proper mechanism is still controversial and suggests multifactorial mechanisms for the development of pressure gradients. The radial-femoral MAP gradient may be caused by a decrease in vascular resistance at the level of the hand28,29, peripheral vasoconstriction30 or a decrease in arterial elastance in the radial artery8. Galluccio et al. determined the demographic or hemodynamic factors driving the radial-femoral MAP gradient in critically ill patients. However, they failed to identify any statistically significant associations, including vasopressor dose or any demographic or hemodynamic data15.
This study showed that patients with MAPradial < 65 mmHg had a moderate correlation and increased bias between radial and femoral MAP and were also associated with significant MAP gradients between both sites. These results suggest that, in patients with marginally maintained MAP, measured at the radial artery, femoral artery catheterization should be considered for accurate arterial blood pressure monitoring in patients with refractory shock31. Monitoring MAP at the femoral artery may avoid future fluid administration or increase of unnecessary vasopressor therapy.
The strength of this study was the use of new statistical analyze to determine bias in the repeated measurement study such as the, bias plot by the Taffé26 and the multilevel mixed-effect model23,24. However, our study had some limitations. First, most patient with refractory shock in this study had septic shock. Therefore, it may have limited generalizability to other types of shocks. Second, we selected patients with refractory shock who received high doses of vasopressors, which may limit extrapolation for patients with less severe shock. Lastly, the clinical impact of arterial sites on morbidities or mortality was not measure in this study. Therefore, a larger study is required to further investigate the impact of radial and femoral arterial blood pressure monitoring in patients with refractory shock for therapeutic management and patient outcomes.